This chapter answers Section G6(v) of the 2017 CICM Primary Syllabus, which expects the exam candidate to "describe the classification of shock". It has appeared in the exams only once, in  Question 13 from the first paper of 2019, where candidates were asked to "classify circulatory shock and provide examples" for 40% of the marks. The rest of the question, like the rest of this chapter, was dedicated to discussing the cardiovascular responses to different shock states. Judging by the pass rate (83%), for the vast majority of ICU trainees this topic is dear and familiar.

In summary:

  • Definition of shock:
    • Failure to deliver and/or utilize adequate amounts of oxygen, leading to tissue dysoxia
  • Classification of shock:
    • Hypovolemic
      • Haemorrhage
      • Water loss (eg. dehydration)
      • Fluid shift
    • Cardiogenic
      • Cardiomyopathy
      • Arrhythmia
      • Mechanical failure (eg. tamponade or valve failure)
    • Distributive
      • Septic/inflammatory vasoplegia 
      • Anaphylaxis
      • Neurogenic shock
    • Obstructive
      • Cardiac tamponade
      • Tension pneumothorax
      • Pulmonary embolism
    • Cytotoxic
      • Mitochondrial toxicity

For the best modern take on shock classification, one should refer to the 2018 article by Standl et al. However, realistically just about any resource would be suitable. The definition and classification of shock are so sufficiently non-controversial that just about every author seems to publish the same information.

Definition of shock

Shock is surprisingly difficult to define. When cornered, most people will either produce a definition which focuses on clinical signs (eg. hypotension) or on some sort of circulatory insufficiency (eg. poor tissue perfusion). If the clinician you have cornered has a poetic bent, they might come out with something like “a momentary pause in the act of death”, which is how  J.C Warren described it in 1895, or "the rude unhinging of the machinery of life", per Samuel Gross (1872). 

The situation is not helped by the fact that the word "shock" is being used outside of its normal lay meaning. Often enough when you look this up, the term is said to come from the French choc, or choquer - by direct translation, “to clash in battle”, a verb which describes the meeting of two warriors in violent conflict. The term is attributed to Henri Francois Le Dran (1685 – 1770), a French surgeon with extensive military experience. He missed out on the Napoleonic wars by about a century, but France was involved in enough action during the 18th century that he had plenty of substrate for practice. He described his experience in an extensive treatise (1743) which outlined the management of projectile injuries, and this book was translated into English by John Clarke, who is often blamed for transliterating "choc" into "shock". In fact, as Millham (2010) points out, he never did any such thing. The terms choc or choquer were actually never used in Le Dran's original work. Where "shock" appears in Clarke's translation, it is used to translate the words saisissementcommotion, and coup; Le Dran was referring to his observation that trauma and blood loss were associated with a certain restless agitation (commotion) or stunning (saisissement), which he interpreted as neurological or psychological phenomena. 

The literature typically assumes that this term was originally applied to describe the systemic effects of a regional injury, which was so violent and war-like that its consequences were rendered systemic:

"...the Bullet, or whatever Body it is, thrown by Gun-powder, acquires such a rapid Force, that the whole animal Machine participates more or less in the Shock and Agitation which is communicated to the Part, the Moment it is struck"

The effect of this sort of military-grade injury was to "seize the whole animal Oeconomy from the Moment of receiving the Wound". Reviewers from the modern era have taken this as a description of systemic organ and tissue effects, whereas it appears Le Dran was referring mainly to the state of profound helpless incomprehension which would be completely understandable in any young man whose arm has just been blown off by cannon fire. In his defence, he also described physiological findings; for example his treatise has chapter headings which describe the clinical features of haemorrhagic shock ("Restlessness and Inquietude", "The inextinguishable and burning Drought""Convulsive and palpitating Pulse", etc). Obviously all sorts of prior authors (eg. Galen) had described horrific injuries, but none had gone to the same length in describing their systemic effects, focusing instead on the anatomy and practical management. 

By this stage, the reader will likely be resentful of their time being wasted, and so without further ado we should quickly move to some pragmatic modern definition. The most widely accepted version probably comes from a 2006 International Consensus Conference (Antonelli et al, 2007).  There, a "jury" of representatives from five critical care societies came together in a Paris hotel room to 

"a life-threatening, generalized maldistribution of blood flow resulting in failure to deliver and/or utilize adequate amounts of oxygen, leading to tissue dysoxia"

This, and in particular the bit about failure to deliver and/or utilize adequate amounts of oxygen is reproduced extensively throughout the literature, and would probably be accepted by the most picky examiners.

Classification systems to describe shock

The scientific purist would ask for a system derived from the definition. And as the definition is "failure to deliver and/or utilise oxygen", it seems like it would be reasonably easy to pull it apart into a classification system. For example, we know all of the determinants of oxygen transport; why not plug them in? Realistically, yes - you could do that - but you end up with a system which does not really help you clinically, and one which places emphasis on the rare and weird causes of shock, while lumping common causes into a small handful of categories. Observe:

Failure to utilise available oxygen

  • Failure of oxidative phosphorylation, eg. cyanide toxity
  • Mitochondrial dysfunction, eg. septic shock

Failure to deliver enough oxygen

  • Increased demand for oxygen
    • Increased metabolic demand (eg. hyperthyroidism, hyperthermia)
    • Hyperthyroidism
  • Inadequate oxygen carrying capacity of the blood
    • Insufficient haemoglobin (eg. anaemia)
    • Insufficient available oxygen (hypoxia)
    • Altered oxygen-haemoglobin interaction (eg. carbon dioxide toxicity)
  • Inadequate cardiac output
    • Inadequate heart rate 
      • Bradycardia
    • Inadequate stroke volume
      • Inadequate preload
        • Low circulating volume (haemorrhage, dehydration)
        • Maldistributed circulating volume (neurogenic shock, anaphylaxis, sepsis, vasoplegia following bypass)
        • Atrial fibrillation (lost atrial kick)
        • Tachycardia with inadequate diastolic filling
        • Obstruction to venous return (tension pneumothorax, cardiac tamponade)
      • Excessive afterload
        • Aortic stenosis or regurgitation 
      • Inadequate ventricular contractility (eg. myocardial infarction, ventricular arrhythmia)

As you can see, anaphylaxis sepsis and neurogenic shock all end up being grouped together somewhere around the "preload" category, whereas cyanide toxicity and hyperthyroidism enjoy a position of undeserved eminence. Thus, this sort of system is not widely accepted for a number of reasons. Instead, medical scientists as a community have agreed to classify shock according to a combination of clinical and biological criteria, preserving only the sort of categories that help describe the aetiology and suggest treatment. Thal & Kinney (1967) seem to be the first to have articulated this sort of system, "to emphasize not only the initiating factors but also the primary physiologic deficit". The best version of it can be found in Standl et al (2019), and is reproduced below with minimal modification. 

  • Hypovolemic
    • Haemorrhage
    • Water loss (eg. dehydration)
    • Fluid shift
  • Cardiogenic
    • Cardiomyopathy
    • Arrhythmia
    • Mechanical failure (eg. tamponade or valve failure)
  • Distributive
    • Septic/inflammatory vasoplegia 
    • Anaphylaxis
    • Neurogenic shock
  • Obstructive
    • Cardiac tamponade
    • Tension pneumothorax
    • Pulmonary embolism
  • Cytotoxic
    • Mitochondrial toxicity

This system is imperfect, but widely accepted and likely to score marks. Many authors have also added cytotoxic shock, though its inclusion is contested among shock nerds because it is not a circulatory phenomenon. One other disadvantage of this classification framework is the failure to account for states where oxygen delivery is inadequate only because the oxygen consumption is unnaturally increased, such as the state of malignant hyperthermia. Most sane people would agree that these concerns represent obsessive nitpicking. As the college answer to Question 13 from the first paper of 2019, 

Cardiovascular responses to shock

The nature of the cardiovascular response to any given shock state will generally depend on what sort of shock state it is, making this a difficult question to answer. Question 13 from the first paper of 2019 attributed 60% of the total marks to "outline the cardiovascular responses". Because the examiners' comments are literally two lines, it is hard to get a detailed impression of what exactly they wanted, but it appears that "sensor, integrator, effector mechanisms were necessary to pass". For lack of a better idea, the content of the cardiac reflexes chapter was remixed with the best of the neurohormonal circulatory control chapter to produce this formatted table:

Cardiovascular Responses to Shock
Stimulus Sensor Integrator Effector mechanism
Hypotension Baroreceptors Nucleus of the solitary tract
  • Vagus (increased heart rate)
  • Sympathetic nervous system (vasoconstriction and increased cardiac output; redistribution of blood flow away from splanchnic circulation and skin)
  • RAAS activation
  • (increased angiotensin levels; vasoconstriction)
Decreased VO2 Aortic arch chemoreceptors Nucleus of the solitary tract
Decreased circulatory volume Atrium (atrial myocytes)
  • Decreased release of atrial natriuretic peptide
Baroreceptors Hypothalamus
  • Increased release of vasopressin; water retention
Renal juxtaglomerular cells
  • Increased release of renin; RAAS activation; aldosterone release; salt retention
Inadequate tissue perfusion Vascular smooth muscle and endothelium
  • Autoregulatory vasodilation (myogenic,  metabolic, and mediated by endothelial vasoactive mediators such as nitric oxide)

References

Le Dran, Henry-François. A Treatise or Reflections Drawn from Practice on Gun-shot Wounds. John Clarke, 1743.

Frost, Paul, and Matthew Wise. "Recognition and management of the patient with shock." Acute medicine 5.2 (2006): 43-47.

Millham, Frederick Heaton. "A brief history of shock." Surgery 148.5 (2010): 1026-1037.

Antonelli, Massimo, et al. "Hemodynamic monitoring in shock and implications for management." Intensive care medicine 33.4 (2007): 575-590.

Standl, Thomas, et al. "The nomenclature, definition and distinction of types of shock." Deutsches Ärzteblatt International 115.45 (2018): 757.

Thal, Alan P., and John M. Kinney. "On the definition and classification of shock." Progress in cardiovascular Diseases 9.6 (1967): 527-557.